Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system

ABSTRACT: Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system

PROVIDER: PRJNA480005 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7478820.fastq.gz	Fastqsanger.gz
	SRR7478821.fastq.gz	Fastqsanger.gz
	SRR7478814.fastq.gz	Fastqsanger.gz
	SRR7478815.fastq.gz	Fastqsanger.gz
	SRR7478816.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system with Vero cells

Project description:Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system with Vero cells

| PRJNA716329 | ENA

Tissue responses to Shiga toxin in human intestinal organoids

Project description:Intestinal tissue responses to protein synthesis inhibition by Shiga toxin are complex. Organoid models allow for an unprecedented examination of human tissue responses to a deadly Shiga toxin.

2020-02-01 | GSE144633 | GEO

Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system

Project description:Isolation of genes whose knockout conferring resistance to STx-Induced cell death

2018-12-20 | GSE116730 | GEO

Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system with Vero cells

Project description:Isolation of genes in Vero cell whose knockout confer resistance to Stx-induced cell death

2021-05-06 | GSE169364 | GEO

Genome-wide essential gene identification for SubAB toxin-induced cell death using CRISPR/CAS9 screening system

Project description:Genome-wide essential gene identification for SubAB toxin-induced cell death using CRISPR/CAS9 screening system

| PRJNA517089 | ENA

Shiga-toxin producing Enterotoxigenic Escherichia coli

Project description:Shiga-toxin producing Enterotoxigenic Escherichia coli

| PRJEB25657 | ENA

Effects of E. coli Shiga toxin on the gene expression profile of human microvascular endothelial cells

Project description:Changes in endothelial phenotype induced by E. coli-derived Shiga toxins (Stx) are believed to play a critical role in the pathogenesis of hemolytic uremic syndrome. Stx inactivate host ribosomes, but also alter gene expression at concentrations that minimally affect global protein synthesis. The effect of Stx on the gene expression profile of human microvascular endothelial cells was examined using the Affymetrix HG-U133A platform. Data were processed using 13 different methods and revealed 369 unique differentially expressed genes, 318 of which were up-regulated and 51 of which were down-regulated. These studies implicated activation of the CXCR4/CXCR7/SDF-1 chemokine pathway in Stx-mediated pathogenesis. Primary human dermal microvascular endothelial cells were treated with vehicle or Shiga toxin (10 fM, 24 h, n = 6) and changes in steady-state mRNA levels were determined by hybridization to Affymetrix HG-U133A arrays

2011-10-10 | E-GEOD-32710 | biostudies-arrayexpress

Genome-wide essential gene identification for SubAB toxin-induced cell death using CRISPR/CAS9 screening system

Project description:Isolation of genes whose knockout confer resistance to SubAB-Induced cell death

2019-04-26 | GSE125650 | GEO

Functional Dissection of the Retrograde Shiga Toxin Trafficking Inhibitor Retro-2

Project description:The retrograde transport inhibitor Retro-2 has a protective effect on cells and in mice against Shiga-like toxins and ricin. Retro-2 causes toxin accumulation in early endosomes, and the relocalization of the Golgi SNARE protein syntaxin-5 to the endoplasmic reticulum. The molecular mechanisms by which this is achieved remain unknown. Here, we show that Retro-2 targets the endoplasmic reticulum exit site component Sec16A, affecting anterograde transport of syntaxin-5 from the endoplasmic reticulum to the Golgi. The formation of canonical SNARE complexes involving syntaxin-5 is not affected in Retro-2-treated cells. In contrast, the interaction of syntaxin-5 with a newly discovered binding partner, the retrograde trafficking chaperone GPP130, is abolished, and we show that GPP130 must indeed bind to syntaxin-5 to drive Shiga toxin transport from endosomes to the Golgi. We thereby identify Sec16A as a druggable target, and provide evidence for a non-SNARE function for syntaxin-5 in interaction with the retrograde cycling protein GPP130. a) Clickable Retro-2 pulldown. To identify protein target of Retro-2.1, providing the first steps to explain effects of Retro-2 on inhibition of STxB retrograde trafficking from endosomes to Golgi. b) GFP-STX5 pulldown. To find interactors of STX5, to build a hypothesis to explain the affect of Retro-2-inhibited anterograde trafficking of STX5 to Golgi, which in turn inhibits STxB retrograde transport from endosomes to Golgi. c) GFP-Sec16A pulldown. The aim of this proteomics assay is to show the effects of Retro-2 on the Sec16A interactome. Results show the differential effects of Retro-2 treatment on the Sec16A interactome, giving insight into the mechanism by which Retro-2, via Sec16A, specifically affects the anterograde trafficking of Syntaxin-5.

2020-02-24 | PXD015642 | Pride

Alterations in gene expression in response to different regimes of Shiga toxin 2

Project description:The microarray data provided here belong to a study that describes two different Shiga toxin (Stx) induced models of hemolytic uremic syndrome (HUS) in mice. Although several rodent models of HUS were published, it still remains difficult to reproduce all clinical features of human HUS. Here, two different Stx2 regimes combined with volume resuscitation were tested in C57BL/6J wild type mice. Animals were euthanized because of kidney injury after 3 or 7 days respectively. Kidneys were removed for histological evaluation and RNA extraction. Kidney injury was confirmed histologically and by laboratory parameters in plasma. Data for the respective vehicle treated groups are also provided here.

2017-10-01 | GSE99229 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data